Barbiturates, phenytoin, ephedrine, carbamazepine, rifampicin, and other drugs that stimulate hepatic metabolism: These drugs may enhance dexamethasone metabolism, shorten its plasma half-life and lead to less effect of dexamethasone. Phenytoin may decrease dexamethasone's bioavailability by over 50%. Increased dexamethasone dosage may be required.
CYP 3A4 inhibitors such as ketoconazole and macrolide antibiotics: May increase plasma concentrations of corticosteroids.
Indinavir, erythromycin and other drugs metabolized by CYP 3A4: Dexamethasone is a moderate inducer of CYP 3A4 and may increase clearance of these drugs, resulting in decreased plasma concentrations.
Oral contraceptive and estrogen: Can cause alterations in plasma protein binding and metabolism of corticosteroids which can result in exposure of women to increased levels of the unbound corticosteroid for long periods of time.
Aspirin: Concomitant use of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids increase the risk of gastrointestinal adverse effects. Use aspirin cautiously in conjunction with corticosteroids in hypoprothrombinemia.
Concomitant administration of dexamethasone and aspirin may also cause changes in salicylate plasma protein binding and its rate of metabolism. These changes cause lowering of plasma salicylate levels.
Warfarin: Coadministration of corticosteroids and warfarin usually result in decreased response to warfarin, although there have been conflicting results. Monitor coagulation indices frequently to maintain the desired anticoagulant effect.
Potassium-depleting agents such as diuretics and amphotericin-B: Observe patients closely for the development of hypokalemia. In addition, there have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure.
Anticholinesterase agents: Concomitant use of anticholinesterase agents and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, withdraw anticholinesterase agents at least 24 hours before initiating corticosteroid therapy.
Antacids: Large doses of antacids can cause a decrease in corticosteroid absorption.
Insulin and Oral Antidiabetic Agents: Concomitant administration of dexamethasone and insulin generally requires higher doses of insulin. Dosage adjustment of antidiabetic agents may be required because corticosteroids may increase blood glucose concentrations.
Ketoconazole: Decreases the metabolism of certain corticosteroids by up to 60% leading to an increased risk of corticosteroid side effects.
Thalidomide: Toxic epidermal necrolysis has been reported when dexamethasone was used concomitantly with thalidomide.
Indomethacin: May cause false negative results in the dexamethasone suppression test (DST).
Aminoglutethimide: May diminish adrenal suppression of dexamethasone.
Cholestyramine: May increase the clearance of dexamethasone.
Ciclosporin: Increased activity of both ciclosporin and corticosteroids may occur when the two are used concurrently. Convulsions have been reported with concurrent use.
Digitalis Glycosides: Patients may be at increased risk of arrhythmias due to hypokalemia.
Ephedrine: May enhance the metabolic clearance of corticosteroids, resulting in decreased blood levels and lessened physiologic activity, thus requiring an increase in corticosteroid dosage.
Other interactions: Toxoids and live or inactivated vaccines: Patients on prolonged corticosteroid therapy may exhibit diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response. Corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. If possible, postpone routine administration of vaccines or toxoids until corticosteroid therapy is discontinued.
Skin tests: Corticosteroids may suppress reactions to skin tests.
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